Neurokinin Receptor 1 (NK1R) Antagonist Aprepitant Enhances Hematoma Clearance by Regulating Microglial Polarization via PKC/p38MAPK/NFκB Pathway After Experimental Intracerebral Hemorrhage in Mice

2021 ◽  
Author(s):  
Peng Jin ◽  
Shuixiang Deng ◽  
Prativa Sherchan ◽  
Yuhui Cui ◽  
Lei Huang ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Microglial Polarization ◽  
Neurokinin Receptor ◽  
Nfκb Pathway

scholarly journals Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

2016 ◽  
Vol 54 (3) ◽  
pp. 1874-1886 ◽  
Author(s):  
Zhen Zhang ◽  
Ze Zhang ◽  
Hong Lu ◽  
Qingwu Yang ◽  
He Wu ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Inflammatory Mediators ◽  
Microglial Polarization

scholarly journals Minocycline promotes posthemorrhagic neurogenesis via M2 microglia polarization via upregulation of the TrkB/BDNF pathway in rats

2018 ◽  
Vol 120 (3) ◽  
pp. 1307-1317 ◽  
Author(s):  
Hongsheng Miao ◽  
Runming Li ◽  
Cong Han ◽  
Xiuzhen Lu ◽  
Hang Zhang
Keyword(s):  
Intracerebral Hemorrhage ◽  
Therapeutic Potential ◽  
Autologous Blood ◽  
Neurological Deficits ◽  
Neuroprotective Effects ◽  
Microglial Polarization ◽  
Arginase 1 ◽  
M2 Microglia ◽  
Microglia Polarization ◽  
Bdnf Pathway

Intracerebral hemorrhage (ICH) is a devastating disease worldwide with increasing mortality. The present study investigated whether minocycline was neuroprotective and induced M2 microglial polarization via upregulation of the TrkB/BDNF pathway after ICH. ICH was induced via injection of autologous blood into 150 Sprague-Dawley rats. A selective TrkB antagonist [N2–2-2-oxoazepan-3-yl amino] carbonyl phenyl benzo (b) thiophene-2-carboxamide (ANA 12)] and agonist [ N-[2-(5-hydroxy-1H-indol-3-yl) ethyl]-2-oxopiperidine-3-carboxamide (HIOC)] were used to investigate the mechanism of minocycline-induced neuroprotection. Minocycline improved ICH-induced neurological deficits and reduced M1 microglia marker protein (CD68, CD16) expression as well as M2 microglial polarization (CD206 and arginase 1 protein). Minocycline administration enhanced microglia-neuron cross talk and promoted the proliferation of neuronal progenitor cells, such as DCX- and Tuj-1-positive cells, 24 h after ICH. Minocycline also increased M2 microglia-derived brain-derived neurotrophic factors (BDNF) and the upstream TrkB pathway. ANA 12 reversed the neuroprotective effects of minocycline. HIOC exhibited the same effects as minocycline and accelerated neurogenesis after ICH. This study demonstrated for the first time that minocycline promoted M2 microglia polarization via upregulation of the TrkB/BDNF pathway and promoted neurogenesis after ICH. This study contributes to our understanding of the therapeutic potential of minocycline in ICH. NEW & NOTEWORTHY The present study gives several novel points: 1) Minocycline promotes neurogenesis after intracerebral hemorrhage in rats. 2) Minocycline induces activated M1 microglia into M2 neurotrophic phenotype. 3) M2 microglia secreting BDNF remodel the damaged neurocircuit.

Abstract 114: CX3CR1-null Microglia Fail to Transition to an M2 Phenotype after Intracerebral Hemorrhage

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Roslyn A Taylor ◽  
Matthew D Hammond ◽  
Youxi Ai ◽  
Lauren H Sansing
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Flow Cytometry ◽  
Intracerebral Hemorrhage ◽  
Microglial Polarization ◽  
Arginase 1 ◽  
The Right ◽  
Bone Marrow Chimeras ◽  
Receptor Cx3cr1 ◽  
M2 Phenotype

Introduction: Intracerebral hemorrhage (ICH) results in the activation of microglia. Microglia can polarize into either a pro-inflammatory (M1), or a reparative (M2) phenotype; the effect of microglial polarization after ICH is unknown. Microglia express the chemokine receptor CX3CR1, which has been shown to regulate microglial neurotoxicity. CX3CR1 +/GFP mice have a functional CX3CR1 and are frequently used to identify microglia. We previously reported that mice with CX3CR1-null microglia do not show functional recovery 14 days after ICH. We hypothesize that 1) microglia transition from M1 to M2 phenotypes in the acute to subacute period after ICH and 2) CX3CR1-null microglia fail to make this transition, inhibiting recovery after ICH. Methods: ICH was modeled by injecting 20ul of WT blood into the right striatum. Microglia were sorted from male CX3CR1 +/GFP mice 0.5, 1, 3, 7, and 14 days after ICH in order to specifically study microglia phenotypes. RNA was extracted and qRT-PCR was performed to analyze changes in gene expression. To study microglial CX3CR1 function, C57BL/6 (WT) and CX3CR1 GFP/GFP (CX3CR1-null) mice were irradiated and reconstituted with WT bone marrow (CD45.1) to generate bone marrow chimeras (CD45.1->WT or CD45.1->CX3CR1-null). Brains were harvested for flow cytometry 14 days after ICH. Results: At 12 hours after ICH, microglia have high IL-6 gene expression (M1). However, M2 markers arginase-1, TGF-β and SOCS3 increase over time (Fig. 1), suggesting microglia transition from M1 to M2 over the first 2 weeks after ICH. By flow cytometry, CX3CR1-null microglia had significantly less SIRPα, a receptor involved in phagocytosis of erythrocytes, and CD206, an M2 marker, than WT microglia 14 days after ICH. Conclusions: Our data show WT microglia transition from an M1 to an M2 phenotype after ICH. Our results also suggest microglial CX3CR1 is necessary for transition toward an M2 phenotype after ICH and this transition is required for recovery after ICH.

scholarly journals Berberine exhibits neuroprotective effects through inhibited autophagy and promoted microglial M1 transferred to M2 polarization

2020 ◽  
Author(s):  
Qiang Lei ◽  
Zhiping Hu ◽  
Binbin Yang ◽  
Zheng Jiang ◽  
Fangfang Zhou
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neuroprotective Effect ◽  
Neurological Deficits ◽  
Current Evidence ◽  
Secondary Injury ◽  
Neuroprotective Effects ◽  
Neurological Outcomes ◽  
Microglial Polarization ◽  
The Brain ◽  
M1 Type

Abstract Background: Intracerebral haemorrhage (ICH) induces autophagy excessive activation and microglia mainly switched into proinflammatory M1 type, which can cause severe secondary injury. Current evidence has implied that berberine has a protective effect against ischaemic stroke through mediated autophagy and microglial polarization. However, the neuroprotective effect of berberine in intracerebral hemorrhage (ICH) remains unclear.Method: In this study the effect of berberine on rats model of intracerebral hemorrhage were investigated through Immunofluorescence, qPCR, ELISA, and western blot.Result: Berberine administration significantly reduces neurological deficits and the brain water content via inhibited autophagy, promoted M1 type microglia to M2 type, and subsequently exerts anti-inflammation effects in a rat model of ICH.Conclusion: These results suggest that berberine reduced secondary injury and improved neurological outcomes in ICH model.

The Role of Stereotactic Technology in the Management of Intracerebral Hemorrhage

1992 ◽  
Vol 3 (3) ◽  
pp. 685-702 ◽  
Author(s):  
Christopher B. Shields ◽  
William A. Friedman
Keyword(s):  
Intracerebral Hemorrhage

Erythropoietin induces neuroprotection in experimental intracerebral hemorrhage via eNOS upregulation and STAT3 activation

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S481-S481
Author(s):  
Soon-Tae Lee ◽  
Kon Chu ◽  
Manho Kim ◽  
Jae-kyu Roh
Keyword(s):  
Intracerebral Hemorrhage

Neuroprotective effect of antisense oligodeoxynucleotides in experimental intracerebral hemorrhage in rats

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S505-S505
Author(s):  
Huijin Yan ◽  
Mengzhou Xue ◽  
Christopher Power ◽  
Marc R Del-Bigio ◽  
James Peeling
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neuroprotective Effect ◽  
Antisense Oligodeoxynucleotides
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